Objective: The objective of this study was to investigate asymmetric synaptic density and glucose consumption in moderate-stage non demented PD patients and the association between these measures.

Background: In addition to the well-known asymmetry seen in motor symptoms and pathology in many PD patients, this patient group exhibit variable degrees of asymmetric hypometabolism. We hypothesize that cortical asymmetric synaptic degeneration (and atrophy) may follow the asymmetric hypometabolism sometimes observed during disease progression, thus leading to similar asymmetric profiles in moderate-stage non-demented PD (nPD) patients.

Method: Using in vivo positron emission tomography (PET) we quantified cerebral synaptic density with [¹¹C]UCB-J PET and cerebral glucose metabolism with [¹⁸F]FDG PET. The novel PET tracer [¹¹C]UCB-J binds to the presynaptic vesicle protein SV2A and has been validated as the first universal synaptic density marker in humans. Individual left and right hemisphere GM volumes-of-interest regions were defined using magnetic resonance T1 scans from 19 nPD patients and an Asymmetry Index (AI) was defined: (R-L)/((R+L)/2).

Results: The main findings included 1) significant correlations between [¹⁸F]FDG AI and [¹¹C]UCB-J AI in 19 nPD patients (Pearson r=0.62, P=0.006), and 2) significant correlation between [¹⁸F]FDG AI and UPDRS-III AI in 19 nPD patients (Spearman r=0.56, P=0.008)

Conclusion: Here, we investigated the relationship between in vivo asymmetric glucose uptake and asymmetric synaptic density. We revealed a link between cortical asymmetric synaptic degeneration, asymmetric motor symptoms (UPDRS-III score) and asymmetric glucose consumption in non demented PD patients.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/asymmetric-synaptic-density-and-glucose-consumption-in-subjects-with-non-demented-parkinsons-disease-as-measured-with-11cucb-j-and-18ffdg-pet/